AI Article Synopsis
- Retinal pathological angiogenesis (PA) is linked to diseases like age-related macular degeneration and diabetic retinopathy, and this study explores the role of the protein biglycan (BGN) in this process using a mouse model.
- The researchers found that BGN levels increased in the retinas of mice with oxygen-induced retinopathy and that inhibiting BGN led to reduced PA, suggesting BGN plays a crucial role in promoting this condition.
- Further analysis indicated that BGN's effect on PA may involve the upregulation of another protein, CXCL12, and blocking the interaction between CXCL12 and its receptor significantly decreased PA in mice, highlighting the importance of pericytes in
Article Abstract
Retinal pathological angiogenesis (PA) is a common hallmark in proliferative retinopathies, including age-related macular degeneration (AMD), proliferative diabetic retinopathy (PDR), and retinopathy of prematurity (ROP). The mechanisms underlying PA is complex and incompletely understood. In this study, we investigated the role of extracellular matrix (ECM) protein biglycan (BGN) in PA using an oxygen-induced retinopathy (OIR) mouse model, along with hypoxia (1% O) conditions for incubating pericytes and endothelial cells in vitro. We found a significant upregulation of Bgn in the retinas of OIR mice. Intravitreal injection of Bgn-specific small interfering RNA (siRNA) in OIR mice at postnatal day 12 (P12) effectively curbed retinal PA at P17. Using cultured cells, we found that BGN expression in pericytes was highly sensitive to hypoxic stimulation compared to endothelial cells. We further showed that BGN stimulated retinal PA via the upregulation of C-X-C motif chemokine ligand 12 (CXCL12). Inhibition of the CXCL12-CXCR4 axis effectively diminished PA in OIR mouse. In conclusion, our study demonstrated the stimulatory role of BGN in retinal PA, identified the link between BGN and CXCL12 expression, and further highlighted the role of pericytes in retinal PA.
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| http://dx.doi.org/10.1096/fj.202401903R | DOI Listing |
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11701870 | PMC |
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